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Mechanism and prevention strategy for mesial temporallobe epilepsy following febrile status convulsion

热态惊厥后颞叶内侧癫痫的发病机制及防治策略

基本信息

批准号：
22591132
负责人：
FUKUDA Mitsumasa
金额：
$ 2.75万
依托单位：
Ehime University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2010
资助国家：
日本
起止时间：
2010 至 2012
项目状态：
已结题

项目摘要

Febrile seizures (FS) are recognized as an antecedent to the development of temporal lobe epilepsy with hippocampal sclerosis (TLE-HS). In this study, we used a rat model of FS to study the effects of inflammatory cytokines on seizure susceptibility and neuronal death in adulthood. Prolonged hyperthermia-induced seizures (pHS) were induced in male Lewis rats on P10 and 12, and IL-1β were administered twice intranasally at the seizures. Adulthood seizure susceptibility (P70) was significantly enhanced in rats receiving IL-1β together with repeated pHS, whereas no significant effects were seen in rats receiving IL-1β after a single pHS episode (P10). Significant hippocampal neuronal cell loss was observed in the CA3 region of rats receiving IL-1β together with repeated pHS. Our results are consistent with the hypothesis that excessive production of IL-1β after repeated prolonged FS could enhance adulthood seizure susceptibility and neuronal cell death, and might contribute tothe development of TLE-HS.

热性惊厥（FS）被认为是颞叶癫痫伴海马硬化（TLE-HS）发展的先决条件。在这项研究中，我们使用FS大鼠模型来研究炎性细胞因子对成年期癫痫易感性和神经元死亡的影响。在P10和P12时，在雄性刘易斯大鼠中诱导延长的高血压诱导的癫痫发作（pHS），并在癫痫发作时鼻内给予IL-1β两次。在多次pHS同时接受IL-1β的大鼠中，成年期癫痫发作易感性（P70）显著增强，而在单次pHS发作后接受IL-1β的大鼠中未观察到显著影响（P10）。在接受IL-1β和重复pHS的大鼠的CA 3区中观察到显著的海马神经元细胞损失。我们的结果与以下假设一致：反复长时间FS后IL-1β的过度产生可增加成年期癫痫发作的易感性和神经元细胞死亡，并可能参与TLE-HS的发生。